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Early onset or syndromic epilepsy v6.7 ANO4 Arina Puzriakova Tag gene-checked tag was added to gene: ANO4.
Early onset or syndromic epilepsy v6.6 ANO4 Achchuthan Shanmugasundram Tag Q2_24_promote_green was removed from gene: ANO4.
Tag Q2_24_MOI was removed from gene: ANO4.
Early onset or syndromic epilepsy v6.6 ANO4 Achchuthan Shanmugasundram reviewed gene: ANO4: Rating: GREEN; Mode of pathogenicity: ; Publications: ; Phenotypes: ; Mode of inheritance: MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown
Early onset or syndromic epilepsy v6.5 ANO4 Achchuthan Shanmugasundram Source NHS GMS was added to ANO4.
Source Expert Review Green was added to ANO4.
Rating Changed from Amber List (moderate evidence) to Green List (high evidence)
Early onset or syndromic epilepsy v5.13 ANO4 Sarah Leigh commented on gene: ANO4: To date, no phenotype has been associated with ANO4 variants in OMIM, Gen2Phen or Mondo.
Early onset or syndromic epilepsy v5.13 ANO4 Sarah Leigh Phenotypes for gene: ANO4 were changed from to sporadic encephalopathic and familial epilepsy
Early onset or syndromic epilepsy v5.12 ANO4 Sarah Leigh Classified gene: ANO4 as Amber List (moderate evidence)
Early onset or syndromic epilepsy v5.12 ANO4 Sarah Leigh Gene: ano4 has been classified as Amber List (Moderate Evidence).
Early onset or syndromic epilepsy v5.11 ANO4 Sarah Leigh gene: ANO4 was added
gene: ANO4 was added to Early onset or syndromic epilepsy. Sources: Literature
Q2_24_promote_green, Q2_24_MOI tags were added to gene: ANO4.
Mode of inheritance for gene: ANO4 was set to MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown
Publications for gene: ANO4 were set to 38744284
Mode of pathogenicity for gene: ANO4 was set to Loss-of-function variants (as defined in pop up message) DO NOT cause this phenotype - please provide details in the comments
Review for gene: ANO4 was set to GREEN
Added comment: PMID: 38744284 reports five de novo ANO4 missense variants in patients (I1–I5) with a phenotype that includes intellectual disability, developmental and epileptic or epileptic encephalopathy (DEE/EE) and hypotonia. A further two ANO4 missenses variants were observed, one had been inherited from unaffected mother (patient F7) and with a penetrance of 73% in members of a large pedigree with a milder phenotype (PMID: 38744284: Supplementary figure S2). Febrile seizures plus (GEFS+) or temporal lobe epilepsy were associated with these inherited variants. A dominant negative mechanism was proposed by Yang et al (PMID: 38744284) as a result of functional studies of one of the variants causing DEE/EE and one causing GEFS+.
Sources: Literature